Background
Accumulating evidences indicate that long non-coding RNAs (lncRNAs) play an important role in initiation and development of thyroid cancer. However, the underlying molecular mechanism remains elusive.
Conclusions
In conclusion, the findings suggest that lncRNA-MIAT may promote PTC proliferation and invasion through physically binding miR-324-3p and upregulation of LASP1.
Methods
To explore potential oncogenic and tumor suppressive lncRNAs in papillary thyroid cancer (PTC), we performed RNA sequencing to discover differentially expression lncRNAs between PTC tissues and matched normal tissues. RT-qPCR was used to validate differentially expressed lncRNAs. Bioinformatic analysis was performed to predicted potential miRNA and gene which might be regulated by MIAT. Cell proliferation, invasion and cycle assay were conducted to study the function of MIAT and LASP1 in PTC.
Results
Through analysis of RNA sequencing, we observed that lncRNA-MIAT was overexpressed in PTC tissues. The upregulation of MIAT was further confirmed in 40 pairs of PTC tissues and normal tissues we collected. In the function assays, results suggested that MIAT silencing led to inhibition of cell proliferation, invasion and disruption of cell cycle progression in PTC cells. Mechanistically, MIAT directly bound to miR-324-3p and upregulated LASP1 expression in PTC cells. In addition, expression of MIAT was positively correlated with LASP1 mRNA expression in samples collected from patients with PTC. More importantly, transfection of recombinant LASP1 attenuated MIAT silencing induced inhibition of cell proliferation, invasion and disruption of cell cycle progression in PTC cells. Conclusions: In